Expert Postings, Apr - Jun 1997

Copyright by Michael Jones, Bill Elkus, Jim Lyles, and Lisa Lewis 1997 - All rights reserved worldwide.
Disclaimer

Table of Contents

 
This file contains postings made by the following professionals: 
 
Karoly Horvath, M.D.--an associate professor of pediatrics at the 
   University of Maryland at Baltimore.  Dr. Horvath set up the 
   Pediatric Gastrointestinal and Nutrition Laboratory, and is now 
   director of this lab. 
 
Donald D. Kasarda, Ph.D.--a research chemist with the United States 
   Department of Agriculture.  Dr. Kasarda has worked on grain proteins 
   in relation to grain quality for 30 years.  He has colloborated with 
   medical groups working on celiac disease for about 25 years and has 
   often been used as an informal consultant by support groups. 
 
Vijay Kumar, M.D.--president of IMMCO Diagnostics, one of the labs that 
   performs celiac antibody blood tests. 
 
Phil Sheard, Ph.D.--researcher in the Developmental Biology Unit, 
   Department of Physiology, University of Otago Medical School, in 
   Dunedin, New Zealand. 
 

Date: Wed, 9 Apr 1997 07:44:49 -0400 From: Karoly Horvath (khorvath@UMABNET.AB.UMD.EDU) Subject: CD & anemia, elevated liver-enzymes and diarrhea Oral iron therapy resistant anemia and elevated liver enzymes can be the first manifestations of celiac disease. It is well known and we try to teach this features of CD to the medical students and residents here at the University of Maryland. An other post concerning the diarrhea, negative serology testing suggests that this child may have celiac disease. There are lot of causes of diarrhea. Furthermore, after a diarrheal disease certain children have a postenteritis syndrome with loose stools for occasionally several weeks. This is generally a self-resolving condition. The disappearence of diarrhea on a gluten-free diet can be a coincidence and would not confirm celiac disease and does not justify a life-time gluten-free diet. If there is any doubt regarding the serology test it is best to do an intestinal biopsy now (and not on a gluten-free diet). This not a medical advice. Karoly Horvath Baltimore ========================================================================= Date: Sat, 12 Apr 1997 08:40:40 -0400 From: Karoly Horvath (khorvath@UMABNET.AB.UMD.edu) Subject: Allergy vs intolerance Allergic reaction is a hyperreaction of immune system to a certain environmental antigen (called allergen), which may manifest on all the surfaces with direct contact to the outside environment such as gastrointestinal tract, lung and skin (or in the blood vessels after the administration of an intravenous drug). By definition this reaction occurs within minutes (hours) and it is the consequence of immunoglobulin E production to this antigen. However, if somebody has had lot of specific IgE immunglobulin to this antigen in the blood, the reaction may occur within minutes after ingesting, inhaling or contacting the allergen. This immunoglobulin binds to special cells (called mast-cells) in the skin or lung or gastrointestinal tract causing the release of different compounds stored in these specialized cells. The release of these compounds (e.g. histamin) causes different skin rashes (e.g angioedema), asthmatic breathing or abdominal cramps with diarrhea. The intolerance term in the gastroenterology means that somebody is not able to tolerate certain food components. It is a wide terminology. First of all, it is not an IgE immunoglobulin-mediated process. There are different mechanisms behind a gastrointestinal intolerances: -The most common is the lactose intolerance, which is the consequence of a decreased enzyme activity (lactase) in the small intestine. Because the lactose is not digested and absorbed in the upper part of the small intestine it goes down to the last part of the intestine and to the colon, where the normal bacterial flora hydrolyzes the lactose. The unabsobed lactose causes a so called osmotic diarrhea. The hydrolysis of lactose sometimes results in only increased gaseoussness with crampy pain. -The gluten-intolerance is a other example. It is an immunoreaction to a fragment of gliadin molecule in the small intestine, but it is not an IgE immunglobulin mediated process. A more complex and different immunological reaction occurs in the upper part of the small intestine, which does not cause immediate symptoms, but slowly damages the segments of the small intestine contacted with the gliadin molecule. As the damage goes down and longer segments of small intestine has the damage (villus atrophy) the symptoms may manifest. -There is a transient intolerance to milk- and soy proteins in infants. It may start within 1-4 weeks on milk or soy containing formulas. It may cause diarrhea and bloody stools. The elimination of these proteins from the diet results in a rapid improvement (within two weeks). From unknown reason this intolerance is temporary only and most of the infants with cow-milk or soy protein intolerance are able to tolerate these proteins without any problem after two years of age. This suggests a temporary immaturity or dysfuction in their gut immune system. I hope this note helps to clarify the difference between allergy and intolerance. Karoly Horvath, M.D. Baltimore ========================================================================= Date: Wed, 16 Apr 1997 14:53:45 -0400 From: George & Gayle Kennedy (gmk3@CORNELL.edu) Subject: is one allergic to wheat or just the gluten? Yesterday I asked for help in knowing whether people who were allergic to wheat were reacting to the whole wheat berry or just to the gluten part of the protein in wheat. Don Kasarda kindly answered the post and has given permission to send this information on to all of you. )From: "Donald D. Kasarda" (kasarda@pw.usda.gov) )Subject: Re: wheat allergy ) )Gayle, ) )Although there may be some controversy about the role of the different types )of reactions in celiac disease, I will give you my current opinion on the )matter for what it is worth. I am neither a physician nor an immunologist )so please take that into consideration--and I will throw in the usual )disclaimer about this not being meant as medical advice. ) )I think that in celiac disease, the reaction is most likely to the gluten )proteins only. Reaction to gluten proteins in celiac disease is not )generally immediate, but sometimes will only be recognized by the patient )when sufficient damage has been done to the intestine to cause malabsorption )of nutrients. This might take a day or two to years depending upon the )individual and the degree to which healing had occurred before re-challenge. )Gliadin is a part of or a fraction of gluten. ) )However, people with allergies (by which I define here as having Type I )immediate hypersensitivity to wheat, presumably mediated by IgE type )immunoglobulins) might be reacting either to gluten proteins or to various )non-gluten proteins found in the wheat grain (the alpha-amylase inhibitors )are one example, and this type of protein occurs in wheat and in other )grains--related proteins occur in rice, for example). There are many )different types of non-gluten proteins in wheat grain, although gluten is )the predominant protein fraction. Reaction can be swift or take a few hours )to become noticeable, but this type of reaction is not usually slow in )developing. ) )Don Kasarda )Albany, California ========================================================================= Date: Sat, 3 May 1997 17:47:33 EDT From: Bill Elkus (Bill_Elkus@JEFCO.COM) Subject: Breastfeeding and celiac Linda Blanchard (linda@CCGS.COM) asked: ) Given that one of the best reasons to breastfeed is that mother's milk ) carries antibodies that get passed on to the baby to help protect ) against disease, is it possible that a celiac mom could "trigger" celiac ) disease in her genetically predisposed babe? In other words, if the ) little one had the gene for celiac's disease, would handing that baby ) the antibodies for celiac disease through the milk cause the baby to ) begin "fighting off" wheat gliadin so that when the babies of celiacs ) wean, they would then pick up fighting off the "grain offenders" ) themselves? Karoly Horvath, one of the two directors of the celiac center at University of Maryland in Baltimore, has generously offered the following reply in a private post to me, and asked that I post it to the List: ------------ BREAST-FEEDING AND CELIAC DISEASE Breast milk contains antibodies against all the antigens the mother's immune system has met prior to or during the pregnancy and has produced antibodies to them. This system is the wisdom of nature and this is the way that mother's milk protects babies from all the antigens (infectious agents, toxins etc ) occurring in the environment where the mother lives. These antigens without this protection may enter the body through the digestive or respiratory systems. The best example is that breast milk protects babies from bacteria causing diarrheas in the underdeveloped countries. The antibodies are produced by the cells (plasma cells) localized in the gut and the lung. These cells are migrating to the lactating breast-tissue for hormonal trigger (enteromammal plasma cell circle) and they continue producing these antibodies in the breast. These antibodies appear in the breast milk. In brief, the breast milk may contain all the antibodies the mother has in her digestive and respiratory systems. The function of these antibodies is to block the entrance of antigens infectious agents, toxins, allergens etc) across the digestive or respiratory tract of babies. In case of CD, it means that if the mother has circulating antibodies to gliadin, these antibodies appear in the milk. If the breast fed baby ingests gliadin (or the mother ingests accidentally and traces of gliadin appear in the milk) the antibodies in the milk blocks the gliadin and it will not able to cross the intestinal wall and meet with the baby's immunosystem. Theoretically, the breast-fed infant do not have any immunoreaction to gliadin. If the mother accidentally ingests gliadin during breast feeding it is likely that the concentration of antigliadin antibodies become higher in the breast milk. To answer the question: the antibodies in breast milk are protective and do not "trigger" celiac disease in genetically predisposed babies. There are several data showing that breast feeding has a protective effect in case of celiac disease. Furthermore, it is well documented that breast feeding in the first year of life decreases the risk of allergies by 50% in babies whose parents have allergies. As far as the reaction after weaning concerned: it is also known that babies may have some reaction (loose stool or spit up or discomfort) transiently after introducing a new food, however, this is a temporary symptom and not allergy or immunoreaction to the food. It is likely that their digestive system should accomodate to the new foods. Karoly Horvath Baltimore ========================================================================= Date: Sun, 4 May 1997 08:48:18 EDT From: Bill Elkus (Bill_Elkus@JEFCO.COM) Subject: Horvath on CD and Neurological Manifestations The following is from Karoly Horvath: Bill Elkus Los Angeles 5/4/97 3:45 AM Subject: Celiac and CNS From: KHORVATH@pol.net There are several case reports and summaries discussing association between celiac disease and different neurological symptoms, although generally it is not clear whether the CNS effect secondary to the intestinal damage (malabsorption and deficiency of nutrients, vitamins trace elements etc) or some direct brain effect. For your information I enclose a few references. Sincerely, Karoly Horvath, M.D. Baltimore ---------------------------- CD and Neurological Manifestations 1. Ackerman Z, Eliashiv S, Reches A, Zimmerman J. Neurological manifestations in celiac disease and vitamin E deficiency [letter]. Journal of Clinical Gastroenterology 1989;11(5):603-5. 2. Banerji NK, Hurwitz LJ. Neurological manifestations in adult steatorrhoea (probable Gluten enteropathy). Journal of the Neurological Sciences 1971;14(2):125-41. 3. Baquero M, Narciso ML, Garcia M, Perla C, Dominguez F. [Celiac disease with occipital calcifications: 2 late cases]. [Spanish]. Medicina Clinica 1995;105(20):781-3. 4. Bernier JJ, Buge A, Rambaud JC, Rancurel G, Hauw JJ, Modigliani R, et al. [Nondeficiency chronic polyneuropathies in celiac disease in adults (2 cases with inflammatory neuromuscular vascularitis)]. [French]. Annales de Medecine Interne 1976;127(10):721-9. 5. Bhatia KP, Brown P, Gregory R, Lennox GG, Manji H, Thompson PD, et al. Progressive myoclonic ataxia associated with coeliac disease. The myoclonus is of cortical origin, but the pathology is in the cerebellum. [Review]. Brain 1995;118(Pt 5):1087-93. 6. Camilleri M, Krausz T, Lewis PD, Hodgson HJ, Pallis CA, Chadwick VS. Malignant histiocytosis and encephalomyeloradiculopathy complicating coeliac disease. Gut 1983;24(5):441-7. 7. Cernibori A, Gobbi G. Partial seizures, cerebral calcifications and celiac disease. Italian Journal of Neurological Sciences 1995;16(3):187-91. 8. Collin P, Pirttila T, Nurmikko T, Somer H, Erila T, Keyrilainen O. Celiac disease, brain atrophy, and dementia [see comments]. Neurology 1991;41(3):372-5. 9. Connolly CE, Kennedy M, Stevens FM, McCarthy CF. Brown bowel syndrome occurring in coeliac disease in the west of Ireland. Scandinavian Journal of Gastroenterology 1994;29(1):91-4. 10. Cooke WT, Smith WT. Neurological disorders associated with adult coeliac disease. Brain 1966;89(4):683-722. 11. Cooke WT. The neurological manifestations of malabsorption. [Review]. Postgraduate Medical Journal 1978;54(637):760-2. 12. Cordonnier M, Robin M, Cornette M, Brassinne A, Pirotte J. [Neurologic complications of celiac disease in adults. Apropos of a case]. [French]. Revue Medicale de Liege 1983;38(21):806-14. 13. Della Cella G, Beluschi C, Cipollina F. [Intracranial calcifications--seizures--celiac disease: a case presentation]. [Italian]. Pediatria Medica e Chirurgica 1991;13(4):427-30. 14. Dzieniszewska-Klepacka L, Kurniewicz-Witczakowa R, Mazurczak T. [Effect of the method of feeding on the physical development of infants born with symptoms of intrauterine dystrophy]. [Polish]. Problemy Medycyny Wieku Rozwojowego 1979;9:12-34. 15. Finelli PF, McEntee WJ, Ambler M, Kestenbaum D. Adult celiac disease presenting as cerebellar syndrome. Neurology 1980;30(3):245-9. 16. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? [see comments]. Lancet 1996;347(8998):369-71. 17. Henriksson KG, Hallert C, Norrby K, Walan A. Polymyositis and adult coeliac disease. Acta Neurologica Scandinavica 1982;65(4):301-19. 18. Kinney HC, Burger PC, Hurwitz BJ, Hijmans JC, Grant JP. Degeneration of the central nervous system associated with celiac disease. Journal of the Neurological Sciences 1982;53(1):9-22. 19. Knutson L, Hallgren R, Ahrenstedt O, Bengtsson U, Lavo B, Lennernas H, et al. [Segmental intestinal perfusion. A "new" technique for human studies]. [Review] [Swedish]. Lakartidningen 1994;91(19):1941-6. 20. Kristoferitsch W, Pointner H. Progressive cerebellar syndrome in adult coeliac disease. Journal of Neurology 1987;234(2):116-8. 21. Larrain F, Danus O. [Neurological and muscular changes in celiac disease]. [Spanish]. Revista Chilena de Pediatria 1977;48(2):91-3. 22. Lu CS, Thompson PD, Quinn NP, Parkes JD, Marsden CD. Ramsay Hunt syndrome and coeliac disease: a new association? [see comments]. Movement Disorders 1986;1(3):209-19. 23. Magaudda A, Dalla Bernardina B, De Marco P, Sfaello Z, Longo M, Colamaria V, et al. Bilateral occipital calcification, epilepsy and coeliac disease: clinical and neuroimaging features of a new syndrome. Journal of Neurology, Neurosurgery & Psychiatry 1993;56(8):885-9. 24. Mauro A, Orsi L, Mortara P, Costa P, Schiffer D. Cerebellar syndrome in adult celiac disease with vitamin E deficiency. Acta Neurologica Scandinavica 1991;84(2):167-70. 25. Mitchell M, Robinson TJ. Gluten sensitivity and neurological dysfunction [letter; comment]. Lancet 1996;347(9005):904. 26. Morris JS, Ajdukiewicz AB, Read AE. Neurological disorders and adult coeliac disease. Gut 1970;11(7):549-54. 27. Morris JS. Neurological disorders and coeliac disease. Tijdschrift voor Gastro-Enterologie 1972;15(2):107-15. 28. Muller AF, Donnelly MT, Smith CM, Grundman MJ, Holmes GK, Toghill PJ. Neurological complications of celiac disease: a rare but continuing problem. [Review]. American Journal of Gastroenterology 1996;91(7):1430-5. 29. Sandyk R, Brennan MJ. Isolated ocular myopathy and celiac disease in childhood. Neurology 1983;33(6):792. 30. Troncone R, Greco L, Auricchio S. Gluten-sensitive enteropathy. [Review]. Pediatric Clinics of North America 1996;43(2):355-73. 31. Unsworth DJ. Gluten sensitivity and neurological dysfunction [letter; comment]. Lancet 1996;347(9005):903-4. 32. Ward ME, Murphy JT, Greenberg GR. Celiac disease and spinocerebellar degeneration with normal vitamin E status. Neurology 1985;35(8):1199-201. ========================================================================= Date: Tue, 6 May 1997 09:53:08 +0000 From: Phil Sheard (phil.sheard@STONEBOW.OTAGO.AC.NZ) Subject: CD & related disorders Hi all, with regard to CD and related disorders, I have done a fair amount of reading on the subject and would like to share my conclusions with you. Many of the studies describing a link between CD and another disorder are case histories of patients presenting with the neurological (or other) disorder, who are subsequently tested and found to have CD. I think it reasonable to assume that, in general, patients with significantly elevated risks of related disorders are either undiagnosed or noncompliant (not adhering to a strict GF diet). I believe that the risk of developing an associated disorder does not fall to that of the non-celiac population immediately on establishment of the GF diet, but may take several years of symptomless GF living to decline to that level. You will appreciate that many celiacs are diagnosed relatively late in life, when a significant amount of undetected neurological damage may already have been done by the time CD is diagnosed. I believe that symptomless compliant celiacs should feel comfortable that their risk of developing neurological (or other) diseases is about the same as the non-celiac population. Note, though, that we are all, statistically at risk. So, for instance, if the prevalence of schizophrenia in the general population is 0.5-1%, then its prevalence among compliant celiacs should also be 0.5-1%. Therefore, some of you may develop neurological disorders in spite of strict adherence to a GF diet, and for the same mysterious (non-CD-related) reasons that non-celiacs may suffer these problems. Hope you find this, my personal interpretation of the literature, helpful. With best wishes Phil Philip Sheard Developmental Biology Unit, Department of Physiology, University of Otago Medical School, Dunedin, New Zealand. Ph (64 3) 479-7344 Fax (64 3) 479-7323 ========================================================================= Date: Wed, 7 May 1997 11:00:00 -0400 From: IMMTEST@AOL.COM Subject: Re: Diagnostic Tests There are various test methods employed for establishing the diagnosis of CD. These include: Histopathology on gut biopsy Serum antibody tests (EMA, ARA and AGA) Absorption test (Xylox absorbtion test) Of these, Xylose absorption test is least specific and it measures the physiological damage to the gut. In light of newer findings, this test is used less and less. The most common test(s) that are employed these days for screening for CD are the antibody tests. Additional information on these tests can be obtained from: IMMCO Diagnostics, Inc. 60 Pineview Drive Buffalo, NY 14228-2120 Vkumar@acsu.buffalo.edu ========================================================================= Date: Fri, 9 May 1997 10:02:26 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.GOV) Subject: Re: destroying gluten in wheat? The heat damage referred to concerns the functional properties of the gluten in breadmaking, but the type of damage that occurs will have no effect on the amino acid sequences in the gluten proteins that cause problems for celiac patients. Heat damaged wheat will remain toxic for celiac patients. It will not, however, have good quality for making leavened products such as yeast breads. The effect likely has to do with changes in the molecular weight distribution of the polymeric glutenin fraction or possibly in the degree of branching of the polymers, which incorporate gluten proteins as monomers through intermolecular disulfide bonding. Don Kasarda Albany, California )I have been given an extract from Farmers Weekly, a UK magazine aimed at the )farming community, issued on 2 August 1996. The article is about heat damage )to wheat, I quote )"Over-drying will effectively destroy gluten and the end-result is a loaf )that does not rise." ) )The author was concerned about the general market, but if the statement is )correct, then would wheat, and other cereals become safe for coeliacs if the )grains were subjected to a high temperature? ) )Judy ========================================================================= Date: Fri, 16 May 1997 09:49:29 -0400 From: IMMTEST@AOL.COM Subject: Re: Selective IgA Deficiency )After reading the expert posting archives, I have questions about selective )IgA deficiency. Has anyone on this list had experience with this? My )serum antibody tests were very low although I sure have enough celiac )symptoms and a historically good response to a g-f diet (yes, one set of )the tests was done after a lengthy gluten challenge)... There are various serum antibody tests for CD. Some of these tests are more specific than others. Even low levels of these specific marker antibodies are of great significance in the diagnosis of CD. The incidence of IgA deficiency in patients with CD is more common than in the normal population. Studies of IgA levels in the blood are used to determine IgA deficiency. If it is found that a patient is IgA deficient, further steps can be taken to assure accurate diagnosis: Celiac patients with IgA deficiency still make antibodies of the IgG class and can be diagnosed thereby. Please check with your doctor concerning the significance of your results. Vijay Kumar ========================================================================= Date: Mon, 26 May 1997 21:05:58 +0000 From: rswd@CYBERHIGHWAY.NET Subject: Reprint Nursing Q & A The following answers a question about Celiac Sprue & breastfeeding: ) Given that one of the best reasons to breastfeed is that mother's milk ) carries antibodies that get passed on to the baby to help protect ) against disease, is it possible that a celiac mom could "trigger" celiac ) disease in her genetically predisposed babe? In other words, if the ) little one had the gene for celiac's disease, would handing that baby ) the antibodies for celiac disease through the milk cause the baby to ) begin "fighting off" wheat gliadin so that when the babies of celiacs ) wean, they would then pick up fighting off the "grain offenders" ) themselves? Karoly Horvath, one of the two directors of the celiac center at University of Maryland in Baltimore, has generously offered the following reply in a private post to me, and asked that I post it to the List: ------------ BREAST-FEEDING AND CELIAC DISEASE Breast milk contains antibodies against all the antigens the mother's immune system has met prior to or during the pregnancy and has produced antibodies to them. This system is the wisdom of nature and this is the way that mother's milk protects babies from all the antigens (infectious agents, toxins etc ) occurring in the environment where the mother lives. These antigens without this protection may enter the body through the digestive or respiratory systems. The best example is that breast milk protects babies from bacteria causing diarrheas in the underdeveloped countries. The antibodies are produced by the cells (plasma cells) localized in the gut and the lung. These cells are migrating to the lactating breast-tissue for hormonal trigger (enteromammal plasma cell circle) and they continue producing these antibodies in the breast. These antibodies appear in the breast milk. In brief, the breast milk may contain all the antibodies the mother has in her digestive and respiratory systems. The function of these antibodies is to block the entrance of antigens infectious agents, toxins, allergens etc) across the digestive or respiratory tract of babies. In case of CD, it means that if the mother has circulating antibodies to gliadin, these antibodies appear in the milk. If the breast fed baby ingests gliadin (or the mother ingests accidentally and traces of gliadin appear in the milk) the antibodies in the milk blocks the gliadin and it will not able to cross the intestinal wall and meet with the baby's immunosystem. Theoretically, the breast-fed infant do not have any immunoreaction to gliadin. If the mother accidentally ingests gliadin during breast feeding it is likely that the concentration of antigliadin antibodies become higher in the breast milk. To answer the question: the antibodies in breast milk are protective and do not "trigger" celiac disease in genetically predisposed babies. There are several data showing that breast feeding has a protective effect in case of celiac disease. Furthermore, it is well documented that breast feeding in the first year of life decreases the risk of allergies by 50% in babies whose parents have allergies. As far as the reaction after weaning concerned: it is also known that babies may have some reaction (loose stool or spit up or discomfort) transiently after introducing a new food, however, this is a temporary symptom and not allergy or immunoreaction to the food. It is likely that their digestive system should accomodate to the new foods. Karoly Horvath Baltimore ========================================================================= Date: Mon, 2 Jun 1997 09:50:40 -0500 From: Joseph Murray (Joseph-Murray@MAIL.INT-MED.UIOWA.edu) Subject: refractory celiac disease A recent poster asked about refractory celiac disease. This is a highly complex area and is the most challenging in dealing with celiac disease. While refractory celiac disease can be defined as a patient with celiac disease whose symptoms do not respond to a gluten free diet there are several important questions and issues in coming to the determination that the patient is really suffering from truly refractory disease. To make the diagnosis conclusively first one most be satisfied that there is not another cause of the problem, though rare there are other conditions that can mimic or coexist with celiac disease and cause continued problems. The second issue is whether the patient is truly gluten free and have they been for long enough to conclude that there has been a failure? To make this determination I have the patient keep a complete and detailed dietary record for 3-4 weeks listing every single item they ate and have them save the wrapper or carton for review. If I or the dietitian feel that there is any possibility of contamination then we exclude that item and wait longer. Sometimes the patient is exposed to a higher risk of gluten contamination by eating out a lot where they do not have true control over the food preparation. We check medications that the patient takes regularily. I also check the endomysial antibodies and gliadin antibodies. These should be negative if the patient has been gluten free for at least 6 months. The gliadin IgG may persist longer but usually its levels drop. If these are positive then that makes me think that they have had significant gluten in the diet in the recent past. ( Note : there still may be gluten in the diet if the test is negative) The original and follow up biopsies should be compared to see if there has been any improvement. Assuming that these criteria are met then one can proceed to consider the patient to have refractory disease. At that point it is important to check for complications such as lymphoma, lymphocyctic colitis and possibly pancreatic insufficiency. I treat the patient with an course of antibiotics and consider adding in pancreatic supplements to see if that will help the patients symptoms. It is only at this point do I consider some suppression of the immune system such as with steroids or some other agent. Rarely then patient may be so ill that one must accelerate the decision to treat with steroids. Steroids are powerful medicines that can be very helpful and even lifesaving in many diseases but have attendent risks that should be discussed prior to use. This is not medical advice and should not be used as such. Joe Murray ========================================================================= Date: Mon, 2 Jun 1997 09:58:08 -0500 From: Joseph Murray (Joseph-Murray@MAIL.INT-MED.UIOWA.edu) Subject: Re: celiac disease and fibromyalgia Muscle and joint pains are common in untreated celiac disease and often get better with a strict gluten free diet. The diagnosis of fibromyalgia is somewhat difficult as it is not very well defined from a pathological view point unlike celiac disease which is. I am unaware that the muscle joint complaints are caused by a nutritional deficiency, though that is possible. Certainly the general malnutrition that is occassionally seen in celiac disease may casue muscle wasting. Vit D def. may cause muscle pain and weakness and is fairly common in newly diagnosed celiac disease. If the person has longstanding CD then the most important thing from the celiac disease point of view is to determine if the gut damage has healed and to see if there is any deficiency state. Other diseases of affecting the musculo skeletal system may be more common in a patient with celiac disease including Lupus, sgojren's syndrome and arthritis of various types. This is not medical advice. Joe Murray Univ of Iowa
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